The heart sounds are relatively brief, discrete auditory vibrations that can be characterised by the intensity (loudness), frequency (pitch), and quality (timbre). The S1 identifies the onset of ventricular systole, and S2 identifies the onset of diastole. These two auscultatory events establish a framework within which other heart sounds and murmurs can be placed and timed. The basic heart sounds are the S1, S2, S3, and S4. Each of these events can be normal or abnormal.
First heart sound (S1) occurs early in ventricular systole. S1 consists of two components. The first major component is associated with closure of the mitral valve and coincides with abrupt arrest of leaflet motion when the cusps reach their fully closed positions.
The origin of the second component is generally assigned to the closure of the tricuspid valve. Because the intensity of S1 depends on the velocity of blood and resultant force of closure of the AV valves, factors that increase the force and velocity of ventricular pressure rise tend to increase the intensity of S1. The position of the AV valves at the onset of systole also affects S1 intensity. If ventricular contraction occurs against a wide open valve, the LV leaflets attain a higher velocity (thus louder S1) than if the valve were partially closed. Second heart sound (S2).
The second heart sound occurs at the end of systole. S2, like S1, has two components. The first component of the second heart sound is designated ‘aortic’ (A2) and the second ‘pulmonic’ (P2).
Since systole (the time of ventricular contraction) is usually shorter than diastole (the time of ventricular relaxation) there is a longer pause between S2 and S1 than between S1 and S2.
S1 is of longer duration and of lower pitch; S2 is of shorter duration and of higher pitch. S1 is usually best heard at the apex; S2 is usually best appreciated in the aortic and pulmonic areas.
The presence of tachycardia or bradycardia may change the above relationships.
The physiologic third heart sound (S3) is a low-pitched vibration occurring in early diastole during the time of rapid ventricular filling. The sound of an S3 is produced by the abrupt transmission of forces to the chest wall when the blood mass enters the right ventricle. An S3 is commonly heard in children and adolescents and in some young adults. When heard after the age of 30, it is called a gallop sound and is a sign of pathology, such as left ventricular failure. The physiologic S3 occurs just after A2 and is best heard at the apex with a patient in the left semilateral position. S3 normally disappears completely when the patient sits or stands or performs any manoeuver that lowers heart rate. Conversely, factors that increase heart rate, such as exercise, tend to accentuate a physiologic S3.
The physiologic fourth heart sound (S4) is a very soft, low-pitched noise occurring in late diastole, just before S1. S4 generation is related to the ventricular filling by atrial systole. Vigorous atrial contraction produces rapid acceleration of blood mass. Associated with this event are vibrations in the left ventricle wall and mitral apparatus which are heard as the S4.
A physiologic S4 may be heard in infants, small children, and adults over the age of 50. It is usually heard only at the apex with the patient placed in the left semilateral position. A physiologic S4 is poorly transmitted and is rarely accompanied by a shock (when the S4 can be felt as well as heard). Wide transmission of a loud S4 associated with a shock is pathologic and is referred to as an S4 gallop.
As in the case of S3, manoeuvers that increase the force and frequency of ventricular contraction will accentuate S4. Conversely, manoeuvers associated with cardiac slowing will diminish S4 intensity.
Aortic ejection clicks are high pitched sounds that occur in early systole. There are no associated accentuating manoeuvers. Intensity is not affected by respiration or patient position. Left sided valvular ejection sounds are heard best in the aortic area, and are not widely transmitted. The ejection click of aortic stenosis is heard best in the mitral area, but is widely transmitted. Aortic ejection clicks are seen in congenital and rheumatic valvular aortic stenosis with a deformed but flexible aortic valve.
Conditions associated with obstruction of the aorta, such as systemic hypertension and coarctation of the aorta, are also associated with aortic ejection clicks.
Pulmonic ejection clicks, like aortic ejection clicks, are high pitched sounds of early systole. Unlike the aortic click, the pulmonic ejection click is heard best in the pulmonic area and is rarely transmitted. The pulmonic ejection click is the only right heart sound that decreases in intensity during inspiration. Pulmonic ejection clicks are often associated with mild to moderate valvular pulmonic stenosis, dilation of the pulmonary artery (as seen in pulmonary hypertension), and tetralogy of Fallot.
Non-ejection clicks are high frequency sounds of mid- to late-systole. Clicks associated with tricuspid valve prolapse (“tricuspid clicks”) are best appreciated along the left lower sternal border. Mitral and tricuspid clicks are sometimes only heard with the patient standing. In this position, the ventricles are smaller and the degree of prolapse of both mitral and tricuspid valves is increased. Having the patient exercise or move to a position other than standing usually diminishes the intensity of both mitral and tricuspid clicks. Inspiration tends to increase the intensity of the tricuspid click.
Mitral clicks, commonly associated with mitral valve prolapse, are heard best in the mitral area and usually are not widely transmitted. Mitral clicks are sometimes only heard with the patient standing. In this position, the ventricles are smaller and the degree of prolapse of the mitral valves is increased. Having the patient exercise or move to a position other than standing usually diminishes the intensity of the clicks.
The opening snap of the mitral valve is heard best midway between the pulmonic and mitral areas. The mitral valve opening snap has a quality similar to the normal heart sounds and is often confused with a splitting S2. The brief, sharp, rather snapping sound is heard shortly after the A2 component of S2. When loud, it is widely transmitted over the entire precordium. Optimum audibility is often achieved by turning the patient to the left lateral position. Standing tends to lower the left atrial pressure and thus increase the A2-OS interval. A soft OS may be intensified after exercise that increases atrial pressure. The A2-OS interval is not altered during different phases of respiration; however, the Mitral Valve Opening Snap is usually loudest on expiration.
The auscultatory characteristics of the Tricuspid Valve Opening Snap resemble those of the Mitral Valve Opening Snap. However, the Tricuspid Valve Opening Snap is louder at the Left Lower Sternal Border or over the xiphoid area. Additionally, the loudness of the Tricuspid Valve Opening Snap usually increases markedly during inspiration, whereas the Mitral Valve Opening Snap is often louder on expiration. The interval between the first component of S2 (A2) and the Tricuspid Valve Opening Snap tends to be longer than the interval between A2 and the Mitral Valve Opening Snap. Sitting up tends to accentuate the Tricuspid Valve Opening Snap.
The site of maximum intensity of a sound or murmur is useful but does not always decide its origin. The direction of selective spread and the effect of respiration are also useful factors to take into account.
i) Mitral valve sounds and murmurs are loudest at the apex (MA), with the patient turned on to the left side;
ii) Tricuspid valve sounds and murmurs are localized to the lower left sternal edge (TA), but spread to the apex if the right ventricle is dilated and the left ventricle rotated posteriorly, e.g. Atrial Septal Defect (ASD);
iii) Aortic valve sounds and murmurs: ejection murmurs are loudest in the aortic area (AA, second right interspace) and at the cardiac apex, and are often transmitted to the carotid arteries in the neck, but a short murmur confined to the neck may be heard in young normal subjects with a big stroke volume; in older subjects it suggests carotid stenosis; regurgitant early diastolic murmurs are usually loudest in the third and fourth left intercoastal spaces at the left sternal edge with the patient leaning forward in expiration; with aortic dilation, however, the murmur is usually maximal in the aortic area;iv) Pulmonary valve sounds and murmurs are loudest in the pulmonary area (PA, third left interspace) but often heard lower; andv) Murmurs over the back: the systolic murmurs of peripheral pulmonary stenosis and coarctation of the aorta are heard maximally over the back; a continuous murmur suggests a communication between the descending aorta and pulmonary circulation.
Heart Murmurs have the following types:
1) Innocent Murmurs are associated with no known abnormality either structural or physiological.
2) Physiological Murmurs are caused by disturbance in the physiology of the circulation, e.g., those related to hyperkinetic state or overactive circulation, excitement, anaemia, fever thyrotoxicosis, pregnancy, cor pulmonale, portal hypertension or beri beri heart disease.3) Relative or Functional Murmurs are caused by structural disorders not involving valves or abnormal cardiac or vascular communications; murmurs caused by dilation of heart chambers or dilation of vessels.4) Organic Murmurs are caused by valvular disease, shunts or narrowed vessels.
A widely used existing device is the stethoscope, by means of which little more than the speed of the heartbeat can be observed. The mechanical working of the heart involves complexity that produces, for example, heart sounds and murmurs, which the doctor must detect and characterise (in terms of, for example, location and timing) if an effective diagnosis is to be made.
Electrocardiograms, on the other hand, provide information on the electrical characteristics of the heart, and not mechanical or structural abnormalities. To analyze and detect such mechanical and structural defects, a 2-D ultrasound echocardiogram machine is required. However, although currently one of the most advanced pieces of equipment for detecting cardiac defects, its cost is typically several thousands of dollars (US). Consequently, such echocardiogram machines are generally available only in sophisticated diagnostic labs or larger hospitals, and thus beyond the means of an ordinary cardiologist or general physician. Further, the complexity of echocardiogram machines is such that well-trained lab technicians are required for their operation.
Without herein suggesting that it forms a part of the common general knowledge, WO 01/62152 discloses a system for analysing heart sounds, in which the sounds are filtered and parsed into a sequence of individual heart cycles. Systolic and sub-systolic intervals are identified, and energy values computed for comparison with threshold levels. However, this document teaches the use only of either wavelet transform analysis or Fourier transform analysis in order to identify individual peaks and hence the systole and diastole, and does not take the energy envelope of the heart signal into account.